Certain polycyclic aromatic hydrocarbons destroy rodent oocytes. Oocyte toxicity follows ovarian metabolism of polycyclic aromatic hydrocarbons to reactive metabolites. Experiments exploring the role of metabolic activation using ovarian aryl hydrocarbon (benzo(a)pyrene) hydroxylase activity (AHH) suggest that AHH activity determines the rate of ovotoxicity but not the extent of oocyte destruction which occurs. The metabolic pathway to the proximate ovotoxin(s) is being explored using oxygenated derivatives of benzo(a)pyrene (BP). The 3-, 6-, 7-, and 9-hydroxy- BP derivatives, the 4,5-oxide, both 4,5-dihydrol-BP derivatives, and the 7,8-oxide were less ovotoxic than BP. The 2-hydroxy and the 7,8-dihydrodiol derivatives were more ovotoxic than BP. As the 2-hydroxy is not formed in vivo the 7,8-dihydrodiol-BP appears to be a proximate ovotoxin. Intraovarian injection of BP destroys oocytes, indicating that ovarian monooxygenases and epoxide hydratases are sufficient to metabolize polycyclic aromatic hydrocarbons to ovotoxic metabolites. Experiments utilizing Rhesus Monkeys suggests that non-human primates are less sensitive than rodents to the ovotoxic effects of BP.